12       REPORT ON THE CIVIL VETERINARY DEPARTMENT, BURMA.

In the cerebellum slight neuronophagia and lymphocytic infiltration
were seen in several cases. No lesions were demonstrated in the
cerebrum or other parts of the brain.

Pathogenesis of Kumri.—Lesions are first initiated in the neurons of
the spinal cord and cerebellum by the action of the infective agent or
toxin. A chronic irritating action sets up a low grade inflammation
which results in slow destruction of some neurons by a process of
neuronophagia. The neurons lose their extra cellular processes, shrink,
become invaded by mononuclear cells, and finally disappear, leaving a
space which is filled up by proliferative glial elements. Localised
hyperæmia and a few haemorrhages occur in the regions where nerve
cell destruction is going on ; and a sparse infiltration with lymphocytes
appears. The axon fibres cannot survive when their parent neurons
are destroyed, and those which originated from affected neurons
undergo demyelinisation and degeneration. They are replaced by
neuroglia and appear as sclerotic areas in the white matter of the cord.

No definite regional correlation has been established histologically
between the neurons affected and the symptoms observed ; the peculiar
selectivity of the causal agent in attacking in every case neurons whose
destruction gives rise to closely similar symptoms is remarkable.
Nerve paths normally carrying impulses of voluntary movement to the
posterior part of the body are destroyed and inco-ordination results.
In clinical cases where the inco-ordination appears suddenly the
destructive process has started simultaneously in a number of neurons
and their nerve paths become non-functional at about the same time.

At a certain stage the process of neuron destruction ceases and the
disease becomes static. The degenerated axon fibres of the cord,
lacking the cellular sheath which peripheral nerves possess, cannot
regenerate and return of function is impossible. In horses with mild
symptoms an improvement in function occurs after a long period ; new
reflex paths have been set up in other nerve fibres and these restore to
some extent normal function.

Aetiology.—No experimental evidence has been obtained to indicate
the presence of a virus, although such a causal agent is suggested by the
histological findings. Sub-inoculations, the majority by the intracerebral
route, of pooled brain and cord suspensions into mice, guinea pigs,
rabbits, dogs and horses have failed to transmit the disease. No
conclusive results have been obtained from attempts to cultivate a virus
upon the chorio-allantoic membrane of the developing chick.

Shirlaw in India has reported successful transmission of Kumri to
laboratory animals but his work could not be confirmed in Burma.
This worker's histological results also differed slightly from those at
Insein, as perivascular infiltrations (cuffing of bloodvessels) were a